Cyanidin-3-glucoside inhibits amyloid β25-35-induced neuronal cell death in cultured rat hippocampal neurons

• Published in: The Korean journal of physiology & pharmacology Vol. 22; no. 6; pp. 689 - 696
• Main Authors: Yang, Ji Seon, Jeon, Sujeong, Yoon, Kee Dong, Yoon, Shin Hee
• Format: Journal Article
• Language: English
• Published: The Korean Physiological Society and The Korean Society of Pharmacology 01.11.2018; 대한약리학회
• Subjects: Original; 약리학
• ISSN: 1226-4512; 2093-3827
• DOI: 10.4196/kjpp.2018.22.6.689

Increasing evidence implicates changes in [Ca 2+ ] i and oxidative stress as causative factors in amyloid beta (Aβ)-induced neuronal cell death. Cyanidin-3-glucoside (C3G), a component of anthocyanin, has been reported to protect against glutamate-induced neuronal cell death by inhibiting Ca 2+ and Zn 2+ signaling. The present study aimed to determine whether C3G exerts a protective effect against Aβ 25–35 -induced neuronal cell death in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague-Dawley rats using MTT assay for cell survival, and caspase-3 assay and digital imaging methods for Ca 2+ , Zn 2+ , MMP and ROS. Treatment with Aβ 25–35 (20 µM) for 48 h induced neuronal cell death in cultured rat pure hippocampal neurons. Treatment with C3G for 48 h significantly increased cell survival. Pretreatment with C3G for 30 min significantly inhibited Aβ 25–35 -induced [Zn 2+ ] i increases as well as [Ca 2+ ] i increases in the cultured rat hippocampal neurons. C3G also significantly inhibited Aβ 25–35 -induced mitochondrial depolarization. C3G also blocked the Aβ 25–35 -induced formation of ROS. In addition, C3G significantly inhibited the Aβ 25–35 -induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid β-induced neuronal cell death by reducing multiple apoptotic signals.